Abstract

&ndps;&ndps;The prevalence of late onset Alzheimer’s disease (AD), one of the most common causes for dementia in elder people, is alarmingly increasing worldwide. Various signaling pathways such as oxidative stress, inflammation, and apoptosis are involved in the formation of amyloid beta (Aβ) and tau proteins which are demonstrated as the hall mark of this irreversible disease. Elevated mammalian
target of rapamycin (mTOR) signaling has been reported in the pathophysiology of many human ailments including AD. mTOR is a
serine-threonine protein kinase in the phosphoinositol/protein kinase B pathway which has role in the cellular growth process and
survival. The effect is mediated through the up regulation of protein synthesis and down regulation of autophagy. mTOR is the catalytic subunit of complexes mTORC1 and mTORC2. mTORC1 regulates the cell growth and metabolism whereas mTORC2 is involved in the organization of cytoskeleton. Overwhelming research on this complex signaling machinery during the last decade revealed that mTORC1 enhances the formation of Aβ and decreases its degradation. Furthermore, mTORC1 increases the synthesis and phosphorylation of tau proteins. Both these neurotoxic compounds cause the synaptic plasticity in the preclinical AD patients. Therefore, regulation of mTORC1 may render beneficial effect in preventing the progression of AD mainly at the early stage. Rapamycin and curcumin were demonstrated as inhibitors of mTORC1 and, thereby, showed neuroprotection in experimental AD models. This review article discusses the role of mTORC1 and the agents that target this complex to prevent the formation and progression of AD.